[Current aspects in the pathogenesis of acute pancreatitis]

Alcohol abuse and gallstones are the most important factors in the pathogenesis of acute pancreatitis. Other factors are less frequent, and in some patients one is unable to identify any risk factor. Even in the most frequent forms of alcoholic or biliary pancreatitis little is known about the cellular and molecular mechanisms which lead to severe pancreatitis. New experimental studies have shown that many biochemical and morphological events are similar in different experimental models of pancreatitis as well as in human disease. These changes include intracellular premature activation of trypsin, blockade of luminal enzyme secretion and appearance of intracellular vacuoles. Although activated trypsin triggers the activation of other proteases, it is not trypsin but other proteases (e.g. elastase, chymotrypsin and phospholipase) which damage the pancreatic acinar cell. These pathogenetic findings may lead to the development of inhibitors which more effectively inhibit the latter cell-toxic proteases and may thereby help to improve the therapy.